Strokes Flashcards

Question

Patent Foramen Ovale (PFO) Related Stroke

Answer 1

* Consider in **young person with no classic risk factors:** HTN, DM, HLD * **Paradoxical embolism** from venous clot across the PFO * Often **thrombophilia** as well: factor V Leiden, prothrombin gene mutation 20210A, protein S, protein C, antithrombin-3 * Can be closed but controversial tx

Answer 2

* **Infarction caused by decreased blood flow** * Most distal vessels first to lose perfusion * Combo of **large vessel stenosis** (carotid, vertebral), **upstream stenosis**, **heart failure** (low CO), and **poor collaterals** * **Post cardiac arrest**: no flow to the brain for minutes, the watershed zones are infarcted first * Locations: * **Cortical border zone infarcts** * Between 2 vessels both with low flow * ACA-MCA ⇒ trunk weakness * MCA-PCA ⇒ if b/l prosopagnosia * **Internal border zone infarcts** * Between superficial and deep vessels off a major artery * MCA-lenticulostriates * PCA-thalamoperforators * ACA-Huebner’s * String of pearls on MRI

Answer 3

* _Hemorrhagic infarcts_ due to **partial or complete venous sinus or cortical vein thrombosis** * Not typical distribution of arterial infarcts ⇒ can be B/L or cross expected arterial boundaries * _See unusual pattern of deficits:_ * Saggital sinus thrombus ⇒ bilateral weakness * More seizures * Papilledema * Headache

Answer 4

* _Combo of edema and ischemia:_ * Blood cannot drain into sinus ⇒ back pressure into thin-walled veins ⇒ **extravasation of RBCs along with infarction** * **Hemorrhagic conversion** common * Especially irritating for the brain ⇒ more likely to induce seizures

Answer 5

* **Post-partum** * **Chemotherapy** * Underlying **infection**, **inflammation**, or **malignancy** * Women on **contraceptives** * **Thrombophilia** (ex. TPO) * **Neurosurgery** ⇒ meningioma resection (damage the venous sinus)

Answer 6

* _Diagnosis:_ * MRI brain w/gadolinium and MR venography * CT brain w/ contrast and CT venography * _Treatment:_ * **Anticoagulation** even though may be a hemorrhagic infarct as likely to progress * Extreme cases of _massive cortical venous sinus thrombosis_: **continuous tPA infusion into the sinus** * Look for underlying cause cancer

Answer 7

* A **transient episode of neurological dysfunction** caused by _focal brain, spinal cord, or retinal ischemia_, **without acute infarction** ⇒ **reversible cerebral ischemia** * Same underlying pathology as stroke but completely reverses * **Higher risk of a subsequent stroke** and if occurs ⅓ will be in the next 48 hours * _Workup:_ MRI shows if infarct, image carotids, echo of heart, EKG monitoring for A. Fib * Most are admitted

Answer 8

* Sx depends on which vessel closes * Clinical presentation often suggests etiology: * Sudden ⇒ embolic * Stuttering ⇒ more thrombotic

Answer 9

Anterior circulation stroke * _Frontal and parietal lobes affected:_ * **Weakness and sensory loss**, arm greater than leg * _If dominant hemisphere_ ⇒ aphasia * _If complete_ ⇒ life threatening * Eyes “looking toward the lesion”

Answer 10

Anterior circulation stroke * _Temporo-parietal_: **Wernicke’s receptive aphasia** * _Frontal_: **Broca’s expressive aphasia** * _Frontal motor strip_: **contralateral weakness** * _Parietal sensory strip_: **contralateral sensory loss** * _Nondominant parietal lobe_: **hemineglect** * _Dominant parietal lobe_: **ideomotor apraxia**

Answer 11

Anterior circulation stroke * Leg greater than arm * Rarer because most have intact anterior communicating artery

Answer 12

* **Vertebral artery disease** causes posterior circulation stokes * Extracranial or intracranial vertebral, basilar and PCA occlusions * See various brainstem stroke syndromes

Answer 13

* **_Medial**_ _**⇒**_ _**motor_** * Very medial: **somatic motor** ⇒ tongue and eye movements * Medial: **branchiomotor** ⇒ facial, jaw, and swallowing and voice muscles * **_Lateral**_ _**⇒**_ _**sensory_** * Lateral: **trigeminal nucleus** ⇒ ipsilateral facial sensation * Far lateral: **special sensory** ⇒ vestibular nuclei (huge representation in medulla and pons), cochlear nucleus

Answer 14

Also medial ⇒ more motor & lateral ⇒ more sensory * _Medial:_ * **Descending motor: corticospinal tract** ⇒ contralateral body weakness (crosses at medullary pyramid) * **Corticobulbar** ⇒ dysarthria * _Medial/Lateral:_ * **Descending sympathetic motor tracts** ⇒ pupil, eyelid, facial sweat ⇒ ipsilateral Horner’s syndrome * _Lateral:_ * **Ascending sensory pain and temperature (STT)** from contralateral body (crosses in cord) ⇒ contralateral anesthesia body * _Far lateral:_ * **Cerebellar connections** (peduncles)

Answer 15

* **Occlusion of the PICA** (posterior inferior cerebellar artery) * Final branch of the vertebral artery before it joins to form the basilar artery * **Can be seen with distal vertebral artery occlusion** * One of the most common brainstem strokes * Often misdiagnosed as inner ear disturbance or gastroenteritis

Answer 16

Classic brainstem infarct involving the **lateral medulla** * *Medial part of lateral medulla* ⇒ motor * _Nucleus ambiguus_ [motor nucleus of vagus] ⇒ palate and larynx → **dysphagia** **and hoarseness** * _Descending sympathetics_ ⇒ **ipsilateral** **Horner’s syndrome (ptosis, miosis, anhidrosis)** * *Lateral part* ⇒ sensory * _Descending nucleus/tract of trigeminal_ ⇒ **ipsilateral loss of pain and temperature from face** * _Spinothalamic tract_ ⇒ **contralateral loss of pain and temperature from body** * _Vestibular nuclei_ ⇒**vertigo, N/V, nystagmus** * *Far lateral*: * _Inferior cerebellar peduncle_ ⇒ **ipsilateral ataxia**

Answer 17

Infarct affects **lateral caudal pons** * _Similar to Wallenberg syndrome except:_ * Also see **tinnitus and hearing loss, facial weakness** * **No motor weakness of swallowing and voice**

Answer 18

* **Lacunar infarcts** from small vessel disease of the **paramedian pontine perforators** * Clinically the same as lacunes higher up in internal capsule * _Motor deficits from corticospinal/ corticobulbar tracts_ ⇒ **limited weakness, dysarthria**

Answer 19

**Larger territory of unilateral pons infarcted** ⇒ “lagoonar infarct” * ↑ Corticospinal / corticobulbar tract involvement ⇒ ↑weakness and dysarthria * If 6^th CN nerve nucleus affected (abducens) ⇒ **cannot move the eyes laterally so the eyes drift medially** * Look away from the lesion ⇒ **“wrong way eyes”** * Vs MCA infarct ⇒ look at the lesion * **Atherosclerosis of basilar artery** knocks off many perforators * Ominous as could next occlude the whole basilar artery

Answer 20

Total basilar artery occlusion ⇒ **total pons infarction** * Causes **Locked In Syndrome** * **Fully awake** (reticular activating system spared - is in the midbrain) * **Quadriplegic except for vertical eye movements and blink** * Both 6^th CN nuclei involved ⇒ no lateral eye movement

Answer 21

**Usually embolic from the vertebral artery or heart** Infarct directly affects _midline aspect of midbrain_ ⇒ **Weber Syndrome** * _CN III nuclei_ ⇒ somatic and parasympathetic motor fibers ⇒ **3rd nerve palsy** * Ipsilateral lateral strabismus * Ptosis * Dilated pupil * Ophthalmoplegia * Loss of accommodation * Loss of pupillary reflex * _Long tract signs:_ * _Corticospinal tract_ ⇒ **contralateral spastic hemiparesis** * _Corticobulbar tract_ ⇒ **contralateral lower face weakness, drooping of the corner of the mouth** * **Leads to clotting into bilateral PCA distributions** * _Occipital lobe_ ⇒ **homonomous hemianopsia** (loss of the same half of vision in both eyes) * _Temporal lobe (hippocampus)_ ⇒ **anterograde amnesia** (cannot learn new info)

Answer 22

Occlusion/infarct _usually due to atherosclerosis_ ⇒ **preceded by crescendo TIAs** * **Vertigo** can be peripheral but can also be due to **ischemia to the vestibular nuclei** * **Hemiparesis/bilateral leg weakness or dysarthria** ⇒ corticospinal and corticobulbar tracts * **Ataxia**: ⇒ cerebellar peduncle/ cerebellum * **Numbness** ⇒ 5^th nerve nucleus, spinothalamic, lemniscus tracts * **Nystagmus** ⇒ non-fatiguing, up-beating * **Diplopia or gaze deviation** ⇒ 6^th nerve nucleus, lateral gaze center * **LOC** ⇒ lower midbrain RAS (reticular activating)

Answer 23

6 Dangerous D’s and 3 Nasty N’s * _6 Dangerous D’s_: * **Dizziness** (spinning feeling = vertigo) * **Dysphagia** (problem swallowing) * **Dystaxia** (unsteady w/ walking or coordination problems w/ limbs) * **Diplopia** (double vision) * **Dysarthria** (slurred speech) * **Drop attacks** (sudden loss of power in the legs with falling) * _3 Nasty N’s_ * **Nausea** * **Numbness** (any part of the body) * **Nystagmus** (jerky vision)

Answer 24

* **± Admin of** **tPA** * **Lower BP only to acceptable range for IV tPA tx**: systolic \< 185, diastolic \< 110 * Consider **thrombectomy** and **transfer** to comprehensive stroke center ⇒ “drip and ship” * Large clots that IV tPA cannot reach * Hyperdense MCA sign on CT * Does not exclude patient from tPA or thrombectomy * Recent trials show that stent retrievers used early better long-term outcomes * **Admission to a stroke unit** * PT and begin regular exercise as tolerated * Reintegration into community

Answer 25

“Clot buster” drug * Given within **3-hour window** of first signs of stroke * Can give at **4.5 hours** in select pts with some exclusions * Careful selection to avoid hemorrhagic conversion: 2.7% risk * 100 patients: 16 benefit, 2.7 harm, the rest no difference * _Tx goals:_ * Recanalize blocked artery * Preserve the ischemic penumbra

Answer 26

_Careful selection needed to avoid hemorrhagic transformation_ ⇒ ↑ morbidity and mortality Preserve ischemic penumbra w/o causing infarct core to bleed * **Inclusion criteria for tPA:** * Any clot based arterial ischemic stroke * Large vessel thrombotic * Small vessel lacunar * Cardioembolic * **Exclusion criteria for tPA:** * On warfarin and PT INR \> 1.6 * Use of novel oral anticoagulants (NOACs) within 48 hours * Major recent surgery * Out of the time window * Early major changes on CT

Answer 27

* **_Admission to a stroke unit:_** * Tx for all stroke patients whether or not getting tPA * Studies show a 10% reduction in morbidity and mortality * **_Stroke order sets including:_** * Avoid aggressive tx of BP to normal during first 1-2 days to **prevent compromise of penumbra** unless getting tPA * **Swallowing evaluation** before PO feeds or meds ⇒ avoid aspiration PNA * **DVT prophylaxis** ⇒ heparin or SCD’s * **Early mobilization, OOB, PT** * **Statin** if LDL \> 100 * Cardiac monitoring to look for A. Fib * **Antiplatelet Rx** prior to D/C unless A. Fib and then **anticoagulation**

Answer 28

**Biggest risk for stroke is already having had one** * Long term BP control and regular follow-up with an internist * Tx diabetes * Smoking cessation * Tx of hyperlipidemia * Avoid heavy regular use of alcohol * Weight loss and dietary modification

Answer 29

**Bleeding in the brain parenchyma due to a ruptured vessel.** Deep vs lobar

Answer 30

Hemorrhagic conversion of a lesion as infarct or tumor.

Answer 31

Rupture of parenchymal bleed into the ventricles generally from hypertensive bleed.

Answer 32

Blood in the subarachnoid space generally from ruptured aneurysm or trauma.

Answer 33

Blood in space between the dura and pia/arachnoid from trauma.

Answer 34

Blood between the calvarium and the dura from trauma.

Answer 35

Blockage of CSF flow due to blood in the ventricular system.

Answer 36

Area surrounding the bleed

Answer 37

* Common cause of disability and death * Estimated annual incidence of 33 people per 100k * 5% die before arrival at medical facilities * For the majority that survive, overall prognosis is grave: * 35% dying within 7 days * 50% by 30 days * Large bleeds have up to 80% mortality * **Expansion in first 1-3 days common** ⇒ when clinical deterioration occurs

Answer 38

* Early treatment of hemorrhage is important * **Aggressive tx of elevated BP** **⇒** **↓** **risk of expansion** * Do not worry about compromising an ischemic penumbra w/ aggressive BP lowering * **Peri-hematoma edema is not an ischemic area**

Answer 39

* The most common and most lethal of bleeds * **Due to small vessel disease** * Damage of endothelium by **chronic HTN** w/ resultant **lipohyalinosis** * Same vessels and pathologic process of lacunes and same distribution * _Small perforating arteries to deep structures_ * **Basal ganglia, internal capsule, thalamus and pons** * Instead of the occlusion that causes lacunar infarcts, there is **vessel rupture causing deep bleeds**

Answer 40

* Surgical removal of deep bleeds not beneficial * **Medical management of increased intracranial pressure** * Osmotic agents to pull fluid out * Hypertonic saline * Mannitol * **NOT** corticosteroids * Useless in cytotoxic edema * Useful in vasogenic from brain tumors * Endoscopic infusion of tPA into clots may help

Answer 41

* **Cerebral herniation** * **Obstructive hydrocephalus** when ventricular extension * Drains often ineffective * Clot off * Blood in ventricle a poor prognostic sign

Answer 42

* _Most important prognostic variable_ ⇒ **level of medical support provided** * Withdrawal of support in pts felt likely to have a poor outcome leads to **self-fulfilling prophecies** * Individual patients in traditionally "poor outcome" categories can have a reasonable neurologic outcome when treated aggressively * Very poor prognosis ⇒ survival might be vegetative ⇒ **therapeutic nihilism** ⇒ affects outcomes * AHA guidelines ⇒ **No DNR in first 48 hours unless advance directive for such**

Answer 43

* **More superficial bleeds**, somewhat better prognosis * Most often due to **cerebral amyloid angiopathy (CAA) or contusion** * **DDx: AVM’s, aneurysm, hemorrhagic transformation of infarct/tumor** * **Often amenable to surgical removal** if mass effect and incipient herniation * Especially when in cerebellum ⇒ temporal lobe near surface and accessible

Answer 44

Widespread deposition of beta amyloid in the small caliber vessels of brain making them more likely to rupture. * **Amyloid in vessel walls** **⇒** **↑** **fragility and liable to rupture** * More superficial vessels * Older patients often have **coexisting Alzheimer’s** * Same amyloid in vessels as in brain parenchyma ⇒ **Amyloid neuritic plaques** * Alzheimer’s not an absolute contraindication for lifesaving superficial clot evacuation * **Microbleeds** * Macro-bleeds often in site of prior microbleed * Presence may increase risk of anticoagulation related bleeds * Exact risk not known

Answer 45

* From **warfarin** used for A. Fib, DVT and prosthetic cardiac valves or **novel anticoagulant (NOAC)** used for A. Fib, DVT * Warfarin reversible w/ vitamin K dependent factors as it antagonizes these * NOACs less easily reversed * Only dabigatran has an antidote * **Timing of restarting anticoagulation especially w/ prosthetic heart valves tricky** * Restart too early and extend bleed * Wait too long and re-stroke

Answer 46

* **Post tPA** * More when protocol violations * Treating over 4.5 hours * Treat supportively like any bleed * No agreed upon reversal agent * **Embolic strokes tend to be hemorrhagic** * Abrupt cut off of flow, ischemic endothelium then partial reestablishment of flow * RBC extravasation and hemorrhagic conversion * **More when large stroke** * **In A. Fib**, wait a week to anti-coagulate to prevent conversion * **Hemorrhagic conversion of primary brain tumor** as glioblastoma or metastasis as melanoma or renal cell CA * Both vascular tumors * **Hemorrhagic conversion of cortical venous infarcts**

Answer 47

* **Often embolic and large infarct** * Ischemia of the vascular endothelium then re-establish flow * **Can be post tPA** * More when protocol violations * Supportive Tx, reversal??? * Prevention * In large stroke from A. Fib, wait 1 week to begin anticoagulation

Answer 48

* Back pressure from **obstructed venous drainage** ⇒ extravasation of RBCs ⇒ hemorrhagic infarct * If due to **sinus thrombosis,** need to anti-coagulate ⇒ ↑ bleeding risk

Answer 49

* _Primary_ * Glioblastoma multiforme (GBM) * Very vascular and necrotic so often bleeds * _Metastatic_ * Especially melanoma, renal cell which are very vascular * Treat w/ **corticosteroids** for **vasogenic edema**

Answer 50

* Mostly in **Circle of Willis** * Most rupture into peri-chiasmatic cistern ⇒ **subarachnoid hemorrhage** * Rarely aneurysm rupture aims into the brain ⇒ **parenchymal bleed** * **Re-rupture common** * Day 3-5 **vasospasm common** * **Multiple strokes and high mortality** * **Need early clipping or coiling of aneurysm** (day 1-2) so hypervolemic/hypertensive therapy can be given without re-rupture before vasospasm sets in * At first may not see aneurysm on angiogram because of arterial spasm * Must repeat angiogram later

Answer 51

_3 most common locations to rupture:_ ## Footnote **Anterior Communicator (ACOM)** **Middle Cerebral Artery (MCA)** **Posterior Communicator (PCOM)**

Answer 52

* **Most common to rupture (40%)** * Adjacent to optic chiasm and mesial basal frontal lobe so neighborhood signs of: * _Visual field defects_ such as **bitemporal heteronymous hemianopsia** * Due to compression of the optic chiasm * **Frontal lobe pathology** * **Change in personality**

Answer 53

* **2^nd most common aneurysm to rupture (34%)** * **Deep in temporal lobe** * Can present as a space occupying lesion causing **temporal lobe seizures** * Can look like brain tumor and attempts at resection = disaster

Answer 54

* **3^rd** **most common site to rupture (20%)** * Runs over the _exiting 3’d nerve_ so neighborhood signs of: * Compressed 3’d nerve w/ **blown pupil and ptosis** and sparing eye movements * “Surgical 3’d”

Answer 55

* **Size over 10 mm** * Under 3mm very unlikely to rupture * **Smoking** * Continued **hypertension** * More in **polycystic kidney disease** and **Marfan** **syndrome**, **Ehlers Danlos syndrome** * **Genetics** * If two 1^st degree family members w/ aneurysm, rest should be screened * Consider coiling if unruptured

Answer 56

* Sometimes warning leak from an aneurysm causes “**sentinel headache**” * _Suspect if_: **worst headache of one’s life, sudden-onset, stiff neck**, **wakes from sleep** * _Imaging:_ CT picks up vast majority of SAH * L/P at discretion of MD * The current consensus is that **structural changes in the aneurysm wall or minor bleeding** could be the factors responsible for the pain

Answer 57

**Direct connection of artery to vein without arterioles or capillaries intervening** * Arterial BP against thin-walled veins * Result is **tendency to catastrophic bleed** * **Extension of AVM** to form many interconnected branches * Difficult to tie off all of them * Like “cutting the head off a medusa * Cut one and 3 more pop-up” * _Treatment:_ **Embolize first** to close as many branches and feeder vessels **prior to surgical** excision

Answer 58

* **Small malformed veins**, low pressure and slow flow * **Often leak but not life-threatening** * Causes **local neurologic dysfunction** that **gradually clears** * E.g. brainstem location might cause dysarthria * Without imaging, can behave like ischemic stroke or multiple sclerosis plaque * Often misdiagnosed as either * **No specific tx and prognosis favorable** * Can be multiple, often familial

Answer 59

* **Coup lesions** * Direct force on brain at point of impact * **Contrecoup** * Brain trauma on opposite side of head to direct trauma as result of brain moving through CSF and slamming into the calvarium * Clues that it is traumatic: soft tissue swelling on exam and CT * Frontal and temporal bones most common * Increasing cause of cerebral bleeds w/ aging population and frequent falls

Answer 60

* ICH is a serious disease w/ **high morbidity and mortality** * Despite poor prognosis of large deep bleeds, **must treat aggressively within 1^st** **48 hours** * Aggressive reduction of BP early standard of care * Neurosurgical input vital, mostly for supportive ICU care * Ventricular drainage when hydrocephalus, herniation * **Most common and most lethal bleeds are hypertensive deep hemorrhages** * **Lobar bleeds more superficial,** can be amenable to surgical resection especially if incipient herniation * Often due to CAA, AVMs, hemorrhagic conversions of infarcts or tumors * **Saccular aneurysm rupture usually causes SAH** * Treated w/ clipping early to allow hypertensive/ hypervolemic therapy during the eventual vasospasm at day 3-7 * **Hemorrhagic conversion of arterial infarcts** more common when large and embolic and seen w/ IV tPA * **Hemorrhagic venous infarct** should be considered when unusual distribution of infarct not following arterial circulation * Consider thrombophilia, either acquired or genetic